Chronic pancreatic inflammation induced by environmental tobacco smoke inhalation in rats

Uwe A. Wittel, Krishan K. Pandey, Mahefatiana Andrianifahanana, Sonny L. Johansson, Diane M. Cullen, Mohammed P. Akhter, Randall E. Brand, Bogdain Prokopczyk, Surinder K. Batra

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Abstract

OBJECTIVE: Despite a strong epidemiological association between cigarette smoking and pancreatic diseases, such as pancreatic cancer and chronic pancreatitis, the effects of long-term cigarette smoke inhalation on the pancreas have not been clearly determined. In the present study, we investigated the effect of cigarette smoke inhalation on the pancreas. METHODS: Thirty-six female Sprague Dawley rats were exposed to two different doses of environmental tobacco smoke averaging 100 mg or 160 mg/m3 total suspended particulate matter (TSP) per m3 for 70 min twice a day for 12 wk. The animals were sacrificed and examined for the effects of tobacco smoke exposure on pancreatic morphology and function. RESULTS: In 58% (7/12) of the animals, exposure to 160 mg/m3 TSP cigarette smoke induced a chronic pancreatic inflammatory process with fibrosis and scarring of pancreatic acinar structures. Animals with fibrotic alterations showed an induction of pancreatic pro-collagen 1 gene expression, and the infiltration of immune cells was accompanied by the expression of the inflammatory mediators MIP-1α, IL-1β, and TGF-β in 33% (4/12) of the animals. Acinar cell stress was manifested by a significant up-regulation of pancreatitis-associated protein expression (PAP) in smoke-exposed animals (smoke-exposed 6,932 ± 1,236 vs control 3,608 ± 305, p <0.05). Possibly contributing to the morphological damage to the exocrine pancreas, the inhalation of cigarette smoke induced trypsinogen and chymotrypsinogen gene expression and, furthermore, reduced pancreatic enzyme content. CONCLUSIONS: This study provides experimental evidence of morphological pancreatic damage induced by the inhalation of cigarette smoke, which is likely to be mediated by alterations of acinar cell function.

Original languageEnglish
Pages (from-to)148-159
Number of pages12
JournalAmerican Journal of Gastroenterology
Volume101
Issue number1
DOIs
StatePublished - Jan 2006

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Smoke
Inhalation
Tobacco
Inflammation
Tobacco Products
Particulate Matter
Acinar Cells
Pancreas
Chymotrypsinogen
Trypsinogen
Gene Expression
Exocrine Pancreas
Pancreatic Diseases
Chronic Pancreatitis
Pancreatic Neoplasms
Interleukin-1
Cicatrix
Sprague Dawley Rats
Fibrosis
Up-Regulation

All Science Journal Classification (ASJC) codes

  • Gastroenterology

Cite this

Wittel, U. A., Pandey, K. K., Andrianifahanana, M., Johansson, S. L., Cullen, D. M., Akhter, M. P., ... Batra, S. K. (2006). Chronic pancreatic inflammation induced by environmental tobacco smoke inhalation in rats. American Journal of Gastroenterology, 101(1), 148-159. https://doi.org/10.1111/j.1572-0241.2006.00405.x

Chronic pancreatic inflammation induced by environmental tobacco smoke inhalation in rats. / Wittel, Uwe A.; Pandey, Krishan K.; Andrianifahanana, Mahefatiana; Johansson, Sonny L.; Cullen, Diane M.; Akhter, Mohammed P.; Brand, Randall E.; Prokopczyk, Bogdain; Batra, Surinder K.

In: American Journal of Gastroenterology, Vol. 101, No. 1, 01.2006, p. 148-159.

Research output: Contribution to journalArticle

Wittel, UA, Pandey, KK, Andrianifahanana, M, Johansson, SL, Cullen, DM, Akhter, MP, Brand, RE, Prokopczyk, B & Batra, SK 2006, 'Chronic pancreatic inflammation induced by environmental tobacco smoke inhalation in rats', American Journal of Gastroenterology, vol. 101, no. 1, pp. 148-159. https://doi.org/10.1111/j.1572-0241.2006.00405.x
Wittel, Uwe A. ; Pandey, Krishan K. ; Andrianifahanana, Mahefatiana ; Johansson, Sonny L. ; Cullen, Diane M. ; Akhter, Mohammed P. ; Brand, Randall E. ; Prokopczyk, Bogdain ; Batra, Surinder K. / Chronic pancreatic inflammation induced by environmental tobacco smoke inhalation in rats. In: American Journal of Gastroenterology. 2006 ; Vol. 101, No. 1. pp. 148-159.
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AU - Pandey, Krishan K.

AU - Andrianifahanana, Mahefatiana

AU - Johansson, Sonny L.

AU - Cullen, Diane M.

AU - Akhter, Mohammed P.

AU - Brand, Randall E.

AU - Prokopczyk, Bogdain

AU - Batra, Surinder K.

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N2 - OBJECTIVE: Despite a strong epidemiological association between cigarette smoking and pancreatic diseases, such as pancreatic cancer and chronic pancreatitis, the effects of long-term cigarette smoke inhalation on the pancreas have not been clearly determined. In the present study, we investigated the effect of cigarette smoke inhalation on the pancreas. METHODS: Thirty-six female Sprague Dawley rats were exposed to two different doses of environmental tobacco smoke averaging 100 mg or 160 mg/m3 total suspended particulate matter (TSP) per m3 for 70 min twice a day for 12 wk. The animals were sacrificed and examined for the effects of tobacco smoke exposure on pancreatic morphology and function. RESULTS: In 58% (7/12) of the animals, exposure to 160 mg/m3 TSP cigarette smoke induced a chronic pancreatic inflammatory process with fibrosis and scarring of pancreatic acinar structures. Animals with fibrotic alterations showed an induction of pancreatic pro-collagen 1 gene expression, and the infiltration of immune cells was accompanied by the expression of the inflammatory mediators MIP-1α, IL-1β, and TGF-β in 33% (4/12) of the animals. Acinar cell stress was manifested by a significant up-regulation of pancreatitis-associated protein expression (PAP) in smoke-exposed animals (smoke-exposed 6,932 ± 1,236 vs control 3,608 ± 305, p <0.05). Possibly contributing to the morphological damage to the exocrine pancreas, the inhalation of cigarette smoke induced trypsinogen and chymotrypsinogen gene expression and, furthermore, reduced pancreatic enzyme content. CONCLUSIONS: This study provides experimental evidence of morphological pancreatic damage induced by the inhalation of cigarette smoke, which is likely to be mediated by alterations of acinar cell function.

AB - OBJECTIVE: Despite a strong epidemiological association between cigarette smoking and pancreatic diseases, such as pancreatic cancer and chronic pancreatitis, the effects of long-term cigarette smoke inhalation on the pancreas have not been clearly determined. In the present study, we investigated the effect of cigarette smoke inhalation on the pancreas. METHODS: Thirty-six female Sprague Dawley rats were exposed to two different doses of environmental tobacco smoke averaging 100 mg or 160 mg/m3 total suspended particulate matter (TSP) per m3 for 70 min twice a day for 12 wk. The animals were sacrificed and examined for the effects of tobacco smoke exposure on pancreatic morphology and function. RESULTS: In 58% (7/12) of the animals, exposure to 160 mg/m3 TSP cigarette smoke induced a chronic pancreatic inflammatory process with fibrosis and scarring of pancreatic acinar structures. Animals with fibrotic alterations showed an induction of pancreatic pro-collagen 1 gene expression, and the infiltration of immune cells was accompanied by the expression of the inflammatory mediators MIP-1α, IL-1β, and TGF-β in 33% (4/12) of the animals. Acinar cell stress was manifested by a significant up-regulation of pancreatitis-associated protein expression (PAP) in smoke-exposed animals (smoke-exposed 6,932 ± 1,236 vs control 3,608 ± 305, p <0.05). Possibly contributing to the morphological damage to the exocrine pancreas, the inhalation of cigarette smoke induced trypsinogen and chymotrypsinogen gene expression and, furthermore, reduced pancreatic enzyme content. CONCLUSIONS: This study provides experimental evidence of morphological pancreatic damage induced by the inhalation of cigarette smoke, which is likely to be mediated by alterations of acinar cell function.

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